Trypanosoma cruzi infection selectively renders parasite specific IgG+ B lymphocytes susceptible to Fas/ FasL mediated fratricide

ZUNIGA, ELINA ISABEL; MOTRAN, CLAUDIA C; MONTES, CAROLINA L; YAGITA, HIDEO; GRUPPI, ADRIANA; ADRIANA GRUPPI

JOURNAL OF IMMUNOLOGY

Año: 2002 vol. 168 p. 3965 - 3965

0022-1767

he control of B cell expansion has been thought to be solely regulated by T lymphocytes. We show in this study that Trypanosoma cruzi infection induces up-regulation of both Fas and Fas ligand (FasL) molecules on B cells and renders them susceptible to B cell-B cell killing (referred to as fratricide throughout this paper) mediated via Fas/FasL. Moreover, by in vivo administration of anti-FasL blocking mAb we demonstrate that Fas-mediated B cell apoptosis is an ongoing process during this parasitic infection. We also provide evidence that B cells that have switched to IgG isotype are the preferential targets of B cell fratricide. More strikingly, this death pathway selectively affects IgG(+) B cells reactive to parasite but not self Ags. Parasite-specific but not self-reactive B cells triggered during this response are rescued after either in vitro or in vivo FasL blockade. Fratricide among parasite-specific IgG(+) B lymphocytes could impair the immune control of T. cruz